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Limbic-cortical imbalance is an established model for the neurobiology of major depressive disorder (MDD), but imaging genetics studies have been contradicting regarding potential risk and resilience mechanisms. Here, we re-assessed previously reported limbic-cortical alterations between MDD relatives and controls in combination with a newly acquired sample of MDD patients and controls, to disentangle pathology, risk, and resilience.
We analyzed functional magnetic resonance imaging data and negative affectivity (NA) of MDD patients (n = 48), unaffected first-degree relatives of MDD patients (n = 49) and controls (n = 109) who performed a faces matching task. Brain response and task-dependent amygdala functional connectivity (FC) were compared between groups and assessed for associations with NA.
Groups did not differ in task-related brain activation but activation in the superior frontal gyrus (SFG) was inversely correlated with NA in patients and controls. Pathology was associated with task-independent decreases of amygdala FC with regions of the default mode network (DMN) and decreased amygdala FC with the medial frontal gyrus during faces matching, potentially reflecting a task-independent DMN predominance and a limbic-cortical disintegration during faces processing in MDD. Risk was associated with task-independent decreases of amygdala-FC with fronto-parietal regions and reduced faces-associated amygdala-fusiform gyrus FC. Resilience corresponded to task-independent increases in amygdala FC with the perigenual anterior cingulate cortex (pgACC) and increased FC between amygdala, pgACC, and SFG during faces matching.
Our results encourage a refinement of the limbic-cortical imbalance model of depression. The validity of proposed risk and resilience markers needs to be tested in prospective studies. Further limitations are discussed.
Patients with borderline personality disorder frequently show non-suicidal self-injury (NSSI). In these patients, NSSI often serves to reduce high levels of stress.
Investigation of neurobiological mechanisms of NSSI in borderline personality disorder
In total, 21 women with borderline personality disorder and 17 healthy controls underwent a stress induction, followed by either an incision into the forearm or a sham treatment. Afterwards participants underwent resting-state functional magnetic resonance imaging while aversive tension, heart rate and heart rate variability were assessed.
We found a significant influence of incision on subjective and objective stress levels with a stronger decrease of aversive tension in the borderline personality disorder group following incision than sham. Amygdala activity decreased more and functional connectivity with superior frontal gyrus normalised after incision in the borderline personality disorder group.
Decreased stress levels and amygdala activity after incision support the assumption of an influence of NSSI on emotion regulation in individuals with borderline personality disorder and aids in understanding why these patients use self-inflicted pain to reduce inner tension.
Andreia Santos, Central Institute of Mental Health Mannheim, Germany,
Andreas Meyer-Lindenberg, Department of Psychiatry and Psychotherapy University of Heidelberg and Central Institute of Mental Health Mannheim, Germany
This chapter reviews imaging studies delineating the unique neuropsychiatric features of Williams-Beuren syndrome (WS), as well as recent advances in investigating the neural substrates of the disorder, which have provided significant contributions to unraveling the impact of a specific genetic defect on brain structure and function. It discusses the clinical, behavioral, cognitive and genetic profiles of WS. Studies using high-resolution magnetic resonance imaging (MRI) have found significant brain differences between WS and typically developing individuals. Significant advances in the understanding of the structural basis of WS have come from the application of voxel-based morphometry (VBM), which allows the study of genetic variation without restriction to anatomical boundaries. Findings of the studies reviewed in the chapter offer a systems-level characterization of genetically mediated abnormalities of neural interactions that can be probed for the identification of single-gene effects on brain maturation.
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